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A case of staphylococcal scalded skin syndrome in a neonate caused by mother-to-child transmission through breast-feeding is reported. Staphylococcus aureus isolates from mother and child were identified using random-amplified polymorphic DNA analysis, which is a simple and rapid method for comparing strains. This study confirms the need to avoid breast-feeding in cases of breast abscess.
Staphylococcal Scalded Skin Syndrome (SSSS) is a disease primarily of young children, characterized by exfoliative dermatitis caused by exfoliative toxin producing Staphylococcus aureus. We had three cases of SSSS with varied dermatological manifestations-diffuse/scarlitiniform erythema, generalized exfoliation, sand paper skin texture, flaccid bullae, erosions, seborrheic dermatitis like scaling and cracking in skin creases which can be confused with other skin conditions. Hence, a high index of suspicion, early diagnosis and prompt treatment is imperative.
UNLABELLED: A previously well, spontaneously breathing premature infant (gestational age 25 weeks, birth weight 364 g, age 74 days) developed staphylococcal scalded skin syndrome (SSSS). A methicillin-sensitive strain of Staphylococcus aureus producing exfoliative toxins A and B (ETA, ETB) was isolated from a gastric aspirate and a pharyngeal swab. The disease recurred with a milder clinical picture 4 weeks later in the same patient while under steroid treatment. Cultures obtained from conjunctiva and pharynx were again positive for S. aureus. A second premature infant in an adjacent ward developed SSSS 2 weeks after the recurrence in the first patient. No other cases were observed thereafter. A total of 25 individuals who had contact with the first patient were screened for staphylococcal colonisation. S.aureus was isolated from the posterior part of the nasal cavity in 8 of the 25 contacts. These strains and the strain of the first patient were evaluated by PCR for the presence of genes encoding ETA and ETB. Expression of toxins was confirmed by gel electrophoresis and Western blot analysis. Purified toxins were injected into newborn mice to confirm toxin activity. Besides the strain isolated from the first patient, only one isolate from the medical staff was positive for the genes encoding ETA and ETB. CONCLUSION: the carrier of this strain had contact with both patients, suggesting that this individual was the vector between the two patients but not necessarily the source of the original infection. Strict infection control measures were implemented and no further spread of the disease occurred.
Prevention of progression of staphylococcal scalded skin syndrome by molluscum contagiosum indicated a possible interference by viral anti-cytokine molecule such as interleukin-18 binding protein.
We report a case of a 71-year-old man with staphylococcal scalded-skin syndrome (SSSS). The patient, with a chronic history of diabetes mellitus, was admitted to our hospital with lumbago, and a diagnosis of renal-cell carcinoma with bone metastasis was made. In hospital he had sudden onset of high fever and erythema, followed by the formation of flaccid bullae and exfoliation, with a positive Nikolsky sign. Methicillin-resistant Staphylococcus aureus (MRSA), producing exfoliative toxin B, was isolated from blood and bile cultures, and Aeromonas hydrophila was isolated from bile culture. Skin biopsy specimen showed a cleavage of the epidermis at the level of the granular layer. The patient was diagnosed as having SSSS and cholecystitis, and was treated with intravenous antibiotics and percutaneous transhepatic gallbladder drainage, which led to recovery. SSSS in adults is usually associated with immunosuppression. A. hydrophila is recognized as an opportunistic pathogen. SSSS should be considered in the differential diagnosis of immunocompromised adult patients with sudden onset of high fever and erythema.
Staphylococcal scalded skin syndrome (SSSS), a generalized exfoliative dermatitis complicating infections by exfoliative toxin-producing strains of Staphylococcus aureus, is rarely observed in adults, especially in those with chronic renal failure. In contrast to the mortality in infants, the mortality in adults is usually high. A case of generalized SSSS in a peritoneal dialysis patient is reported. A-62-year old Japanese man in whom peritoneal dialysis had been carried out was admitted to our hospital with acute peritonitis. It was intractable peritonitis in terms of resistance to various antibiotics; however, improvement of the peritonitis was shown after the injection of vancomycin. Nine days after the completion of this medication, erythema appeared in the eyes and mouth, and around the nostrils, with an exothermic reaction at 39.0 degrees C. Radial cracks formed in the face within a few days, and the erythema rapidly expanded to the neck, axilla, the whole body. The blood pressure was also lowered, and this led to a state of shock. Culture of skin biopsy specimens yielded identical strains of S. aureus. A presumptive diagnosis of SSSS was made. The patient was treated with antibiotics that were effective against the organisms and with both fluid supplementation and dopamine, resulting in subsidence of the signs and symptoms. The exothermic reaction and skin symptoms were improved promptly, with improvement in the general condition, including the state of shock. This appears to be the first reported case of SSSS caused by S. aureusin an adult patient with peritoneal dialysis who was treated successfully. It is very important that SSSS be differentiated from toxic epidermal necrosis, as the treatment is different.
Over a three-month period, 13 neonates developed staphylococcal scalded skin syndrome (SSSS) in a maternity unit, between four and 18 days after their birth. An epidemiological and descriptive study followed by a case-control study was performed. A case was defined as a neonate with blistering or peeling skin, and exfoliative toxin A Staphylococcus aureus positive cultures. Controls were selected at random from the asymptomatic, non-colonized neonates born on the same day as the cases. All staff members and all neonates born during the outbreak period were screened for carriage by nasal swabs and umbilical swabs, respectively. S. aureus isolates were polymerase chain reaction (PCR) screened for etA gene and genotyped by pulsed-field gel electrophoresis (PFGE). Two clusters of eight and five cases were identified. Receiving more than one early umbilical care procedure by the same ancillary nurse was the only risk factor identified in the case-control study (odds ratio=15, 95% confidence intervals 2-328). The ancillary nurse suffered from chronic dermatitis on her hands that favoured S. aureus carriage. Exfoliative-toxin-A-producing strains, as evidenced by PCR and indistinguishable by PFGE, were isolated from all but one of the SSSS cases, from four asymptomatic neonates, from two staff members and from the ancillary nurse's hands. Removal of the ancillary nurse from duty, infection control measures (isolation precautions, chlorhexidine handwashing and barrier protections), and treatment of the carriers (nasal mupirocin and chlorhexidine showers) led to control of the epidemic. In conclusion, this study emphasizes the need for tight surveillance of chronic dermatitis in healthcare workers.
Over a period of 2 months, 12 babies born in the maternity unit at Guy's Hospital developed staphylococcal scalded skin syndrome in two distinct outbreaks. Staphylococci isolated from the babies, together with those from the mothers and attending medical staff were phage-typed. All isolates from the babies were of type 3A/3C. During the first outbreak only one carrier of the epidemic strain (a paediatrician) was found but a further 12 persons were identified as possible carriers during the second outbreak. In order to confirm the link between outbreaks, all phage group II isolates were subjected to reverse phage-typing, testing for metal-ion resistance, plasmid profiling and in-vivo testing for production of epidermolytic toxin. It was shown that the same epidemic strain of toxin-producing Staphylococcus aureus was responsible for both outbreaks. The affected neonates responded rapidly to a short course of intravenous flucloxacillin. The outbreak ceased after appropriate treatment of all carriers and the implementation of an extensive disinfection policy within the maternity unit.
Exfoliative toxin A, produced by Staphylococcus aureus, causes blisters in bullous impetigo and its more generalized form, staphylococcal scalded-skin syndrome. The toxin shows exquisite specificity in causing loss of cell adhesion only in the superficial epidermis. Although exfoliative toxin A has the structure of a serine protease, a target protein has not been identified. Desmoglein (Dsg) 1, a desmosomal cadherin that mediates cell-cell adhesion, may be the target of exfoliative toxin A, because it is the target of autoantibodies in pemphigus foliaceus, in which blisters form with identical tissue specificity and histology. We show here that exfoliative toxin A cleaved mouse and human Dsg1, but not closely related cadherins such as Dsg3. We demonstrate this specific cleavage in cell culture, in neonatal mouse skin and with recombinant Dsg1, and conclude that Dsg1 is the specific receptor for exfoliative toxin A cleavage. This unique proteolytic attack on the desmosome causes a blister just below the stratum corneum, which forms the epidermal barrier, presumably allowing the bacteria in bullous impetigo to proliferate and spread beneath this barrier.
Exfoliative skin diseases of the neonate are relatively rare but when present require rapid diagnosis and treatment to decrease morbidity and mortality associated with these entities. We present the case of a 795 g premature male infant who developed exfoliative lesions on day of life 66. Skin and blood cultures were obtained and intravenous antibiotics initiated. Results of a Tzanck smear suggested toxic epidermal necrolysis (TEN), so the infant was emergently transferred to a local children's hospital with burn unit capabilities for further care. Further histopathological evaluation of the skin biopsy confirmed the diagnosis of staphylococcal scalded-skin syndrome (SSSS). The desquamation ceased 24 h after the initiation of antibiotic therapy, and the skin lesions resolved within 10 days. We discuss the pathogenesis of SSSS and TEN and highlight the importance of early diagnosis so appropriate treatment can be initiated.
Staphylococcal scalded skin syndrome describes a spectrum of superficial blistering skin disorders caused by the exfoliative toxins of Staphylococcus aureus. In its severe form, the exfoliation can spread to cover the entire body surface area. Two S. aureus exfoliative toxin serotypes affecting humans have been identified, but their purpose and mechanism of action have remained elusive. Based on their interaction with human and mouse epidermis, their three-dimensional structure and site-directed mutagenesis studies, it is speculated that they act as atypical serine proteases, and desmoglein-1 has now been identified as the specific epidermal substrate. Recent studies also suggest that the toxins may have a unique superantigenic activity. Clinically, new rapid diagnostic tests have been developed, including one that is able to detect the toxins directly from serum. With early diagnosis and appropriate management, mortality in children remains low and long-term complications are rare because the lesions are superficial and heal rapidly without scarring. In adults, however, the condition carries a mortality of almost 60% despite aggressive treatment, usually because of serious underlying illness. The recent developments in our understanding of the exfoliative toxins should lead to new and improved diagnostic and therapeutic strategies, including the use of specific antixoxins to prevent exfoliation.
Staphylococcal scalded skin syndrome (SSSS), not previously recorded as a chronic disease, persisted for 2 years in a 50-year-old woman with epilepsy and cerebellar ataxia. Lesions initially suggestive of erythema multiforme and toxic epidermal necrolysis evolved over 2 years into those typical for SSSS, with extensive erosions and subcorneal blisters, showing an epidermal split at the granular cell layer. Exfoliatin A-producing phage I-III Staphylococcus aureus, previously linked only to acute mild adult cases of SSSS, was cultured from purulent discharge in the patient's eyes, ears and open skin lesions. The roles of epilepsy and antiepileptic medications are discussed as possible predisposing factors.
We report the first adult case of staphylococcal scalded skin syndrome (SSSS) due to methicillin-resistant Staphylococcus aureus (MRSA). This case is particularly unusual as the MRSA produced toxic shock syndrome toxin 1 and enterotoxin, but not exfoliatoxin. SSSS was originally described in neonates and is thought to result from exfoliatins which produce subcorneal splitting of the epidermis and are only produced by certain strains of S. aureus. This case reflects the range of toxins that can be associated with SSSS and the clinical manifestations of MRSA infection in adult patients.
An idiopathic disease involving skin and kidneys was seen in two Merino lambs from the same herd. A generalized skin exfoliation in association with acute renal failure were the most prominent clinical features. The condition resembled staphylococcal scalded-skin syndrome of man, and pure cultures of Staphylococcus aureus were isolated from the lesion. Acute renal failure was diagnosed by clinical, biochemical and histological criteria, and necropsy.
A 60-year-old woman with psoriasis vulgaris treated with oral cyclosporin and acitretin developed an acute generalized pustular eruption with erythema and associated fever consistent with acute generalized pustular psoriasis. She was admitted to hospital and, despite intravenous fluid replacement, developed acute renal failure. In addition, she developed staphylococcal septicaemia. After transfer to the intensive care unit because of deteriorating renal function, a sudden onset of widespread flaccid blistering (Nikolsky sign positive) and superficial erosions was noted. Histology of a biopsied blister revealed subcorneal splitting of the epidermis consistent with staphylococcal scalded skin syndrome. The patient was treated with intravenous dicloxacillin and the blistering gradually improved over 10 days.
Staphylococcal scalded skin syndrome (SSSS) may cause significant morbidity in children. It is common practice for adhesive occlusive dressings to be used to apply topical local anaesthetic prior to venepuncture. We report two cases in which removal of these dressings from children with SSSS caused injury and discomfort in areas previously free from blistering. We recommend that an alternative method of topical anaesthetic application is used to minimize skin trauma in these patients.
We report a male infant with onset of an extensive bullous eruption at the age of 45 days. Staphylococcal scalded skin syndrome (SSSS) was suspected. Bullous mastocytosis was diagnosed by cytodiagnosis and confirmed by histologic examination. Three serious relapses were noted in a 2-year follow-up, and SSSS was again suspected because of high fever and leukocytosis with neutrophilia in an infectious context. Cytodiagnosis revealed the presence of mast cells and permitted rapid diagnosis of recurrences of bullous mastocytosis. Systemic corticotherapy dramatically improved the cutaneous lesions and general symptoms. This case report emphasizes the utility of cytodiagnosis in extensive blistering diseases in infancy and the possibility of obtaining rapid healing by using steroids.
Staphylococcal scalded skin syndrome is the term used for a spectrum of primarily neonatal blistering skin diseases caused by the exfoliative toxins, ETA and ETB, of Staphylococcus aureus. Despite 25 y of research, the toxins' mechanism of action is still poorly understood, although evidence suggests that they may act as serine proteases. In this study, 0.1 mg purified ETA isolated from a baby with pemphigus neonatorum was incubated with A431 cells (a human squamous cell line) at 37 degrees C for 8, 24 and 48 h and the supernatant tested for protease activity using azocasein as a non-specific substrate. Phosphate-buffered saline was also incubated as negative control. Incubation of ETA with A431 cells for 48 h resulted in a four-fold increase in supernatant azocaseinolytic activity compared with buffer and cells, ETA alone and buffer alone (p < 0.001). Furthermore, this proteolytic activity was inhibited by PMSF (p < 0.001), a specific serine protease inhibitor. These results provide further evidence for the role of the exfoliative toxins as serine proteases. Furthermore, the A431 cell assay provides a simpler, quicker, cheaper and more acceptable alternative to neonatal mouse epidermis to study the mechanism of action of the exfoliative toxins.